Innate Pharma SA (IPHA) 2021 Q2 法說會逐字稿

Good day, and thank you for standing by, and welcome to the Innate Pharma half year results conference call. (Operator Instructions)

Now I would like to hand the conference over to your speaker, Mondher Mahjoubi. Please go ahead.

Thank you. Good morning. Good afternoon, and welcome everyone. Really, pleasure to be here with you today. This morning, we issued a press release providing a business update for the first half of 2021. I look forward to explaining the progress we've made during the year-to-date as well as address some future goals and milestones. The press release and today's presentation are both available on the IR section of our website.

And before we start on Slide 2, I would like to remind you that we'll make forward-looking statements regarding the financial outlook in addition to regulatory and product plan development. These statements are subject to risks and uncertainties that may cause actual results to differ from those forecasted.

On today's call, I'm delighted to be joined by Dr. Joyson Karakunnel, EVP and Chief Medical Officer; and our CFO, Frederic Lombard, who will present an update, followed by a Q&A session.

On Slide 4, you have the classic intro slide of Innate Pharma. As you know, we are pioneers in the field of innate immunity, and in particular, in NK cells. We follow the science to develop innovative therapeutics for patients, leveraging our know-how and antibody generation platform. We are using this expertise to develop a robust pipeline of novel medicines for cancer.

Please move to Slide 5. Our pipeline shows how we have translated this scientific leadership into robust portfolio of both proprietary and partnered assets. It also illustrate how we are executing against our strategy with our lead asset, lacutamab, supported by partnered and also earlier stage product. Additionally, we have a rich pipeline, including an adenosine pathway with an anti-CD73 an anti-CD39 in the clinic. And the pool of preclinical projects including our ANKET NK cell engager platform, which we will carefully select and bring forth and fuel our clinical pipeline.

Please move to Slide 6. Our strategy centers around 3 core priorities, while we look to drive value from our early R&D efforts through later stage partnerships where it makes sense to do so. First, we look to create near-term value driven by our lead proprietary product candidate, lacutamab, which is in development for T-cell lymphoma. Second, fueling our pipeline and creating longer-term value by leveraging our antibody engineering capabilities to develop innovative molecules with the primary focus on our multi-specific NK cell engager platform delivered from our proprietary ANKET platform. And third, we are building a strong and sustainable foundation for our business, leveraging various partnerships across industry and academia. We will look to partner including a late stage when it makes sense to do so. This will further validate our science and also capital that you can reinvest to advance our early portfolio.

During the first half of this year, we have worked diligently to execute against these 3 core priorities. Number one, we have continued to advance lacutamab as we pursue broad development strategy across T-cell lymphoma. We were excited to showcase lacutamab data in mycosis fungoides from the Phase 2 TELLOMAK trial at Lugano, and we have progressed to Stage 2 earlier than anticipated. In addition, we announced our step-wise approach in developing lacutamab in PTCL with 2 clinical studies for KIR3DL2-expressing patient with the relapsed peripheral T-cell lymphoma, including a randomized controlled trial in collaboration with our partner at the LYSA or Lymphoma Study Association.

We have also worked hard to advance our R&D efforts with our early stage program moving forward. And we were pleased to announce earlier this year that Sanofi made the decision to progress IPH6101, our lead NK cell engager into IND-enabling studies. This is the first candidate to emerge from our multi-specific ANKET NK cell engager platform, and we are very excited by the prospect of this technology, which we believe will fuel our pipeline well into the future. We look forward to telling you more about our progress here later in this call and in the near future. Lastly, we look for further updates on our monalizumab collaboration with data from the randomized Phase 2 COAST trial in Stage 3 unresectable non-small cell lung cancer, which will be presented at ESMO this week.

I would like now to pass the call over to Joyson, who will review the progress made with our portfolio, starting with lacutamab, our lead proprietary asset. Joyson?

On Slide 7, let me start with lacutamab, our first-in-class humanized monoclonal antibody that targets the immune receptor, KIR3DL2. As you may remember, KIR3DL2 is an inhibitory receptor found in approximately 65% of patients across all cutaneous T-cell lymphomas and even more in certain aggressive subtype, but with limited expression and healthy tissue. To date, data from lacutamab have shown promise, demonstrating compelling, single-agent activity and offering immense potential in lymphomas historically associated with the poor prognosis for which there are few therapeutic options at an advanced stage.

On Slide 8, I just wanted to remind you of our development strategy for lacutamab in T-cell lymphoma. We are pursuing a fast-to-market strategy with a potentially pivotal trial underway in the niche setting of Sezary Syndrome where lacutamab was granted U.S. Fast Track designation EU Prime designation last year. We are also looking to potentially expand past Sezary Syndrome to mycosis fungoides where we have encouraging preliminary data from our Phase 3 trial, which I'll cover in a minute. Finally, we are advancing into peripheral T-cell lymphomas with a couple of recently announced trials.

On Slide 9, let me highlight the great progress we have made this year in our ongoing Phase 2 TELLOMAK study for Sezary Syndrome and mycosis fungoides. In mycosis fungoides, firstly, we moved the KIR3DL2-expressing cohort from Stage 1 to Stage 2, clearing a predetermined threshold before 50% of the cohort was enrolled. The KIR3DL2 MF data was also presented at Lugano with the next MF data due in 2022. For the Sezary Syndrome cohort, enrollment is on track, and we expect to be able to report top line data in 2022.

On Slide 10, we have a summary of the cohort 2 mycosis fungoides data in KIR3DL2 expressers. Here we see the preliminary results of cohort 2, which showed an overall response rate of 35% in these late-line patients with limited treatment options. You see the median follow-up is still short, 4.8 months. It is important to consider that there are quite a lot of confirmed responses, and we now have 6 confirmed responses out of 17. And you see that some patients have quite a long duration of follow-up in this cohort 2.

If we look at the response by compartment in the skin, you see that the responses are quite high, now with a 11 confirmed responses out of 17. These skin results are extremely interesting because skin is very important for quality of life of the patient. And so it is interesting to see that the majority of patients had represented a very good complete or partial response in the skin. We are encouraged by the data and look forward to further proof points in 2022.

On Slide 11, as mentioned, we are working to advance our recently announced clinical development plan for peripheral T-cell lymphoma, which will focus initially on the relapsed setting where the unmet medical need is most significant. We are initiating our Phase 1b trial evaluating lacutamab as a monotherapy by mid-year. The study will enroll approximately 20 patients and will evaluate safety and characterize clinical outcome. First data are expected in 2022.

Separately, our partner, LYSA, are initiating an investigator-sponsored Phase 2 study to evaluate lacutamab in combination with the chemotherapy GEMOX. This study will be a multi-center, randomized trial with approximately 60 relapsed/refractory patients outside the U.S. We believe that this step-wise approach will prove efficient in identifying the optimal regimen for lacutamab in the relapsed PTCL study. Depending upon the data generated in these initial studies, we will consider initiating a separate trial in combination with another standard of care treatment. And eventually, we would look to move lacutamab into earlier lines of treatment, including as potential combination in the CHOP regimen in the frontline PTCL or as a consolidation therapy following standard first line.

Moving on to Slide number 12. We are pleased to have presented our latest innovation to our proprietary multi-specific NK cell engager platform that we call ANKET, which Eric Vivier presented at the FOCIS meeting in June, and for which an oral presentation has been accepted for ESMO this week.

ANKET stands for antibody-based NK cell engagement therapeutics. And these multi-specific molecules are made of various building blocks, as is illustrated here. The reason why we are so excited about the ANKET is because we are announcing 2 breakthroughs; first, a technological breakthrough; and second, an efficacy breakthrough. This is leading to the harnessing of NK cell effector function against cancer and also provides proliferation.

So on the technological breakthrough, as you can see on this slide, ANKET is very versatile fit-for-purpose technology that is creating an entirely new class of tri and tetra-specific molecules to induce strategic immunity against cancer. On the efficacy breakthrough, this unique NK cell engager engages for the first time to activating NK cell receptors, namely NKp46 and CD16, but also the combination of receptors for IL-2, IL-2R beta and IL-2R gamma with the IL-2 variant and tumor antigen in a single tetra-specific molecule. Overall, it demonstrates a better anti-tumor efficacy and clinically approved antibodies within the limit of preclinical model.

On Slide 13 is a summary of the data on our recent generation of tetra-specific ANKET, which is made of 4 components; in yellow, an antibody fragment that recognizes the tumor antigen; in green, an antibody fragment that recognizes and NKp46; and in red, an FC quotient that will interact with CD16; and then in blue, a variant of the interleukin-2, IL-2 variant.

On the left side of the graph, we show you the contribution of the tetra-specific ANKET with the IL-2 variant. The black graph on the far left is the vector. The green graph is the tetra-specific ANKET. And the red graph on the right is a tri-specific ANKET with the IL-2 variants separated. You can see the benefit from the green graph in the middle of including the tetra-specific ANKET with the IL-2 variant.

On the right, you can see the benefit of tetra-specific versus the vehicle obinutuzumab in lung mouse models. On the top, you have the vehicle, in the middle tetra-specific ANKET and on the bottom, the CD20 obinutuzumab. Activity is seen with the tetra-specific model that is not seen with obinutuzumab. We look forward to updates on ANKET this year at ESMO and other scientific congresses and look forward to progressing our partnership with Sanofi.

Finally, on Slide 14, we have our third pillar of our strategy of building sustainable business. I wanted to highlight the latest developments for monalizumab, which we have out-licensed to AstraZeneca and received EUR400 million in milestones to date with further potential milestones due. To remind you, monalizumab is an anti-NKG2A, which acts upon the checkpoint pathway to potentiate NK cell activation. This is being trialed in combination with cetuximab in head and neck cancer and also in combination with the anti-PD-L1 immunotherapy durvalumab in lung cancer.

In head and neck cancer, the Phase 3 INTERLINK-1 trial of monalizumab plus cetuximab in IO pretreated head and neck cancer is underway. In addition, we are expecting data from cohort 3 of the Phase 2 trial later this year for the triplet of monalizumab plus durvalumab plus cetuximab in first-line head and neck cancer. As mentioned previously, the Phase 2 data in Stage 3 non-small cell lung cancer COAST trial for monalizumab in combination with durvalumab will be presented at ESMO this week by AstraZeneca. In summary, we look to work further with our partners at AstraZeneca.

I will now hand over to Frederic to cover the financials for the half.

So moving to the finance Slide 15, I will start with one of our key metrics, as usual, our cash position. Our cash and cash equivalents amounted to EUR159.4 million as of June 30 this year, down from EUR181.7 million at the end of Q1 2021. We are in a strong financial position with cash to fund planned operation through at least 2022. In addition, as you can see, we are efficiently managing our resources and sizing opportunity to accelerate our impact by nimbly following data to explore strategic and opportunistic indications. We believe this approach ensures that we remain in position to strategically invest in our vision for Innate.

Now going into the P&L, I will only comment on the main and non-significant lines, and you have very detailed comments in the appendix of the press release that you can refer to for more information. I'll start with our revenue from collaboration. So our revenue and other income amounted to EUR15.7 million and the main resulted from revenues from collaboration and licensing agreements, and to a lesser extent, from governmental funding. This revenue mainly results from the spreading of the upfront and upturn payments received from AstraZeneca for monalizumab, which I'll remind are recognized on the basis of the percentage of completion of the work performed by the company. I'll also remind you that it has no impact on cash.

On operating expenses, so for the first half of 2021, they amounted to EUR41.1 million, a reduction of 11% from the first half of 2020. R&D expenses decreased by EUR9.7 million to EUR21.8 million, representing just over half of our operating expenses. This change mainly results from a decrease in depreciation and amortization expenses allocated to R&D, following the end of the transition period with AstraZeneca in September 2020. Also, the return of commercialization rights in the U.S. and Europe for Lumoxiti as well as the end of the recruitment in trials evaluating avdoralimab in oncology.

Turning to SG&A expenses, they increased by EUR4.8 million to EUR19.3 million for the period, primarily as a result of the provision for charges booked relating to the payment of US$6.2 million to be made to AstraZeneca in April 2022 under the Lumoxiti transition and termination agreement. This is less than the company reported up to US$12.8 million contingent liability at the end of 2020, which was linked to the split of certain manufacturing costs. As such, net income from distribution agreements was nil following the end of the transition period relating to the commercialization of Lumoxiti in the U.S. The company recognized US$1 million net sales of Lumoxiti for the first half of 2021.

With that, I will turn back to Mondher.

So please move to Slide 16. As you can see, we are working diligently to execute across all our strategic pillars and believe that we are laying the foundation to drive near and long-term value for our patients and our shareholders. Looking at our clinical program, we expect to achieve a number of milestones over the next 18 months.

As you've heard from Joyson, our Phase 2 TELLOMAK study for lacutamab continues to progress. And we expect to report potentially pivotal data in Sezary Syndrome and in mycosis fungoides in 2022. In addition, we are moving our PTCL program into the clinic with initial data expected as well in the next year.

For monalizumab, we look forward to the Phase 2 COAST data at ESMO this Friday, which built on the hypothesis of adding monalizumab to the anti-PD-L1 durvalumab. Later this year, as you've heard Joyson, we will present the data from cohort 3 of the Phase 2 in head and neck cancer study, just in the combination of monalizumab, with cetuximab and durvalumab in IO-naive patients with advanced head and neck cancer.

We are further advancing the adenosine pathway agents in the clinic where we are starting a new Phase 1 trial for IPH5301, the anti-CD73, and we look forward to data from the anti-CD39 IPH5201 due in 2022. In parallel, we continue to develop our ANKET technology platform, and we are very encouraged by the preclinical results from our next-generation NK cell engagements. We believe that this represents a natural evolution of our platform, illustrating the potential for all of NK cells and the fact that they could become the next-generation off-the-shelf cancer immunotherapy, with more to come, as Joyson said, this Saturday at an oral presentation at ESMO by Eric Vivier. We look forward to further updates on the progress of our ANKET platform in the second half of this year.

Please move to the conclusion slide, Slide number 17. So as you can tell, we have an exciting journey ahead at Innate. We continue to build our business to create value for patients and stakeholders. And in summary, we have positioned Innate Pharma for the future with this best strategy and made meaningful progress throughout the year. Just to recap in summary, lacutamab, we moved forward with our MF trial and presented new collision data at Lugano. Next year, we will have data on MF and potentially pivotal data in Sezary Syndrome. And we will start with PTCL trials.

Second, our R&D engine was further validated as Sanofi choose to progress IPH6101 into IND-enabling studies. We will continue to leverage this antibody capability to develop innovative molecules with the primary focus on our next-generation ANKET NK cell engager molecules as also demonstrated at FOCIS and ESMO this year.

And finally, as you heard from Joyson, we continue to build the sustainable business by balancing our portfolio with partnered assets that provide substantial revenue stream to support our continued investment in early R&D. Collectively, we are driving value across our business and ultimately advancing our goal to deliver innovative medicines to patients. We look forward to keeping you updated on our progress.

With that, that concludes the prepared remarks, and I will now open the call to questions. Operator?

(Operator Instructions) We're taking our first question from the line of Daina Graybosch.

Two for me. One, just thinking ahead for the monalizumab data to be presented on Saturday, I wonder if you could remind us how much overlap in efficacy and read-through from concept to proof-of-concept study? Do you believe there is when you combine monalizumab, durvalumab versus cetuximab? Does either of these therapeutic combinations or mechanism provides the activities at CD8 cells or NK cells? And then in addition, keeping alive my (inaudible), could we see NeoCOAST data this half? I noticed it's not on your milestone slide, but maybe you don't have specific visibility, just wondering of the possibility outcome.

I'm going to repeat the question because the line was not so great. So to make sure that I got it right and everyone also can hear them. So you asked question on the NeoCOAST data, when this data will be public. And your first question was about the potential read-across or read-through from the COAST data to the INTERLINK trial and the combination of monalizumab with cetuximab. Am I repeating correctly of it?

Correct.

So I'll start with the second question very quickly to say that, as you know, the NeoCOAST data is run by AstraZeneca, it's sponsored and run by AstraZeneca. We have really no further information than what is publicly available on the AZ side, which is that the data are expected in the second half of 2021. So you will hear more probably from AZ in the near future.

With regard to your first question, I think this is an excellent opportunity also for us to remind you our strategy from the basic research, and the slide that Joyson showed to illustrate his remarks on monalizumab, you have 2 mechanisms of action that we have developed in our lab. The first one is a way to enhance the efficacy of antibodies that like cetuximab could have a synergistic effect when combined with monalizumab, and that's what's led to the head and neck program and the Phase 3 trial that was started last year.

And the second piece of information and piece of data that was published already in Cell in 2019 was basically the preclinical package that supported the clinical program of the combination of monalizumab and anti-PD-1 or PD-L1, showing the clear synergy coming from the fact that, as you know, NKG2A is not only expressed on NK cells, but also on a subset of CD8-positive T-cells.

So first of all, I think the 2 trials and the 2 setting and the 2 type of combination are supported by strong scientific rationale. Now as you know better then, these are 2 different tumor types and 2 different settings, and it's really premature to, first of all, speculate on the data before the COAST data presented. And of course, I would be very cautious not to have cross-trial comparison or read across. But I'll hand over to Joyson who can maybe complete this answer.

I think Mondher has summed it up very nicely. I think the strength of the preclinical data that supported these trials both with cetuximab as well as with durvalumab have 2 different mechanisms of action that we look for the combination potentials. We've already kind of seen some of that with head and neck, and we'll have to wait for the data to see what happens with COAST.

I think second, I think Mondher pointed it out very nicely, which is these are 2 different indications, 2 very different settings; 1 adjuvant, the other metastatic. And it would be hard to kind of read across the trials or read across trial comparisons, not only because we try not to do that, but also just because of the differences in indications, settings as well as mechanisms of action.

Does it answered your question, Daina?

Yes, it does.

We are taking our next question from the line of Yigal Nochomovitz at Citigroup.

Mondher and team, I just had a few questions. So first, I know, obviously, you can't disclose the data yet on the ORR and PFS for COAST ahead of the late-breaking presentation. But that said, to the extent that you can comment generally, what percent improvement in ORR and PFS would you view as clinically meaningful benefit for monalizumab plus durvalumab combo over durvalumab monotherapy?

Again, we look forward to seeing the full data presented at ESMO. As you know, it's an oral late-breaking abstract. This was detailed by AstraZeneca at their curtain raiser. They will report ORR, but they'll also present PFS data for both arms, durvalumab plus monalizumab and durvalumab plus oleclumab as the standard of care. I think the design of the trial is well known. It has been already publicly disclosed. It's a well-controlled phase -- randomized Phase 2 trial. They have not, to my knowledge, publicly disclosed the details of the statistical hypothesis.

But I believe what is interesting to have in mind is that these are patients who finished their chemo radiation therapy and are randomized within 6 weeks if they do not progress. And they are being treated with durva-mono or durva-oleclumab for up to 12 months. The response rate is certainly a very important endpoint and is the primary endpoint for this trial. But the quality of the response, and in particular, the disease-free survival or the progression-free survival is certainly something to look at as well. So I believe the response rate is certainly important to assess, and we look forward to seeing this data, but I think the PFS is something closer keep in mind.

And then a second question I had on lacutamab, can you talk a bit about how you're planning to identify Sezary Syndrome and mycosis fungoides patients given that in the major pharma markets, U.S., Europe and Japan, there are only 200 Sezary patients and about 3,000 mycosis fungoides patients according to the SEER database.

Just to make sure I get your question. Is it vis-a-vis the commercial opportunity or talking in general about how we are designing and implementing or executing our clinical trial?

No, more about the commercial opportunity that you find.

This is of course a great question and gives me the opportunity to go back to our strategy. I think the Sezary Syndrome indication came as a prototype indication, if I can say, to validate the mechanism of action since the majority of these patients are expressing KIR3DL2. And we have seen in the Phase 1 basically from the first dose level that when you target this tumor antigen in KIR3DL2, you get a significant tumor shrinkage and even an improvement in quality of life.

I think the Sezary Symptom itself is the first step and I should say the fast-to-market strategy in order to really get those Fast Track designation and Prime designation and exchange with the FDA and with the EMA in order to accelerate the clinical development. The intent of course is to expand beyond that. And the mycosis fungoides is half of the PTCL, as you know. You are right; I mean mycosis fungoides accounts for about 3,500 to max 4,000 new patients every year in the U.S. and in Europe and Japan. And there are about 4,000 non-mycosis fungoides cutaneous T-cell lymphoma.

So all in all, we're talking about up to 8,000 patients with cutaneous T-cell lymphoma, half of them would express the KIR3DL2. And again, the mycosis fungoides segment is not the end of the story. It's certainly much more attractive and much more compelling business case.

But of course, the -- I think the most important milestone of the Lugano meeting was that we have been able to show that lacutamab works outside Sezary Syndrome and it works in T-cell lymphoma, which express the KIR3DL2, which of course solidify, if I may say, the scientific rationale to expand now to peripheral T-cell lymphoma, where the business case stands of course with more than 18,000 new cases every year, peripheral T-cell lymphoma has a much more attractive commercial prospect. But again, the step-wise approach is to validate the mechanism of action, check that this is not a Sezary Syndrome drug, but it works outside Sezary Syndrome, which we are exploring and validating as we speak in TELLOMAK and then go peripheral T-cell lymphoma. And then when you look at the totality of the business case, it's no longer a niche indication, it's a significant market opportunity.

And just I had one final question. This one might be good for Eric or Joyson. I'm just curious about the ANKET platform and the sources of combining NKp46 CD16 and IL-2 are? So is the thought that this tetra-specific asset would be better suited to solid tumors or to hematologic malignancies or are both categories under consideration?

That's another excellent question that of course we debate internally. And I'll hand over to Joyson to sum up the thought behind the selection of the tumor antigen for this multi-specific antibody. Joyson?

So I mean -- so I'm going to kind of go back and talk a little bit about the ANKET platform. And the amazing thing about the ANKET platform is it's very versatile. So as you were stating the NKp46 CD16 attachments to the NK cells with the IL-2 variant in the same, but the tumor antigen is what I call as removable. You could kind of put different tumor antigens in there. This allows for that flexibility. And as Mondher said, there's heavy debates going on internally to determine sort of what is the best approach. We are looking at both solid tumors as well as hematologic tumors. So the versatility of the platform allows for us to kind of really have those debates internally to see which would be the best opportunity either in solid or hematological malignancies.

(Operator Instructions) We are taking our next question from the line of Graig Suvannavejh at Goldman Sachs.

I've got a couple. First is actually on 5301. Certainly, we'll be interested to see what the oleclumab data is for the AstraZeneca compound. But could you remind us how to think about differences that you are aware of between their asset and your assets? So that's my first question around 5301.

And then the second of all, as it relates to the COAST data, anything, at least from a scientific or biological rationale that would help us think about how to think about monalizumab and the efficacy and safety that we might see relative to a CD73 targeted assets such as oleclumab? So that's the second question.

And then maybe just a question on the P&L. How should we think about trending over the next several quarters just given the many moving parts? And in that context, as we think about your current cash balance where you say you have cash at least until 2022, I mean, we're right around the corner. So how is the company thinking about financing options? What kind of options are available? And what's the strategy?

Graig, very important and good questions as usual. I'll start with the first one then hand over to Joyson for the COAST and the mechanistic approach we're thinking about, in particular, with regard to the potential combination with an anti-CD73. And then I'll give the opportunity to our new CFO, Frederic, to address your question about the financing moving forward.

Very briefly on 5301. So as you said, I mean, we do really look forward to seeing the oleclumab data. I remind you other than those data, actually, I'm not aware -- we are not aware of other public randomized data in this field. Everyone remember the BMS and the AZ Phase 1b data presented about 2 years ago at ASCO and AACR showing some trend of activity, but nothing since then. So clearly, the results of the COAST trial with regard to oleclumab arm are of major interest for us and for the other companies that are playing in this field.

Number two, I remind you that we published that data. And again, we have even presented this data at AACR back in 2019, if my memory is correct, comparing our anti-CD73 with the BMS and the AZ once. And clearly, when it comes to the antiemetic activity, our antibody is much better. It's superior in doing the job of blocking the anti-CD73.

Of course, we have to translate those preclinical strengthen into clinical benefit for patients. And that's why we were, to some extent, waiting to see some data emerge in order to try to learn from others. And we have been working over the last couple of months in transforming the IND that we filed at the end of last year into clinical trial, which is about to start, and that would be our first clinical trial testing and assessing IPH5301.

We have a plan on what combination approach we should do. And of course, we look forward to seeing the data from the COAST trial to further fine-tune and also maximize the opportunity around our anti-CD73. That's my answer for your first question.

Now Joyson, the question around COAST. How do we think to the extent, of course, I don't want to speculate on the data, but the mechanism of action and the potential combinability with an anti-CD73 if the 2 arms are effective?

So I think I'll go back and also state the mechanisms of action here clearly are, as we know, are different. So one is in anti-CD73, one is in anti-NKG2A, one, we're looking to see -- I mean, we have preclinical data that has supported ADCC synergy and then finally, with monalizumab, it's non-redundant pathway mechanism of action in combination.

So I think when we look at this, we see 2 -- once again, 2 different tumor types. I mean 2 different -- I mean, same setting, but 2 different mechanism of actions that do have different potentials.

I think when it comes to the clinical data; I think we'll have to wait to see what the COAST data shows. But I would just say these are 2 very distinct mechanism of actions operating in 2 different ways; one, sort of -- sorry, both of them relieving immune suppression. And sorry, I just missed up the cetuximab question, but this was CD73. So with CD73, it's basically the leaving of the tumor, the amount of adenosine that's present, so really decreasing immune suppression. So decreasing adenosine is one, the other one is decreasing 2 different pathways; one, anti-NKG2A and the other one with PD-1.

So I think with that, we'd have to wait for the clinical data to see what's happening. I know that was a little round about a step answer. So I'm happy to repeat it because I think it might had I had cetuximab, and I was like, this is the cetuximab. So clearly, I'm excited about both of these. And I'm like sitting here going, okay. But yeah, in short, the CD73 is adenosine. You're really stopping adenosine synthesis. And so because of that, relieving the immune suppression. The other is 2 pathways, one acting on T-cells, the other one on NK cells. And so I think the clinical data will speak for at least which pathway will be better. I think that last answer is the one I would kind of go versus my first.

Frederic, would you want to take the question on what's the plan and the financing of the company moving forward?

As I said before, the cash position is quite robust at the moment, with EUR159 million. We constantly monitor our financial needs, and we provide an update when needed. We cannot communicate at this stage. In terms of plan, for sure, if you look at the cash burning for this first half versus last year, we see a big decrease, but it's not following this investment on our side. We keep our plan as planned, let's say. Last year was having some special cash burn related to Lumoxiti and special payments that we had at the same time. So today, you will see a slight increase in the second half due to the delivery of some studies that we are having in the pipeline.

And then just in terms of how you're thinking about potential options to extend the cash runway?

At the moment, first of all, we -- Mondher, do you want to...

No, no, please go ahead.

So the different options are; we look at the market, for sure. We look at financing options also with some banks as well. But more than ever, we look how progressing the way we operate and see what we can get out of the partnerships.

So Graig, long story short, we have a solid cash position. And we've been actually -- we have a pretty good track record on making sure that our cash cover, the multiple catalysts and milestones that we have ahead of us because we constantly monitor our financing needs, and we'll provide an update when needed.

We have one question from Arthur He from HCV (sic) [H. C. Wainwright].

So I just wonder one question on the monalizumab for the data going to be reported for the IO-naive patients later this year. So could you remind us what kind of data set we could expect? And how many patients we could look into the data?

Joyson, would you like to answer or I can take it?

Go ahead, Mondher.

So first of all, to remind everyone, this is a single-arm study that test the triplet combination. And again, we -- as I said in my answer to the first question, we have those 2 mechanism of action. We know that monalizumab could be synergistic with antibody that have or act within ADCC, and that's the combination with cetuximab. We know that monalizumab is synergistic with an anti-PD-L1, and the COAST data were based on that rational. I think the triplet is simply the combination of both cetuximab and durvalumab to see whether we can have an increase in response and in quality of response in terms of durability.

So the study was designed really first of all to assess the safety of the triplet because this -- I remind you, this is the first I believe ever triplet IO to be developed or triplet of non-cytotoxic or chemo-free regimen to be developed in head and neck cancer. The safety was good in the first 20 patients. So we expanded the trial to 40 patients. But yet, it's still a single arm trial in advanced, relapsed or metastatic patient with squamous cell carcinoma of the head and neck, who might have been pretreated with chemotherapy or radiation therapy, but who are naive of any PDX treatment.

The data will be presented at the end of the year, and we are looking at the totality of the data with AZ to really determine what's the platform. As you know, the competitive landscape is evolving, and it's important to take into consideration and see the specific unmet need and where we can position this triplet. And again, I insist on the fact that today the standard of care is pembro, plus or minus chemo-dependent on the level of CPS, and the results that we are presenting at the end of the year will be looked at also from that perspective, CPS more than 1 versus the CPS low or PD-L1-negative. And we will be delighted to share this data, as I said, towards the end of the year.

Congratulations on the progress.

There are no further questions on the phone.

Henry, do we have question on the webcast?

No more questions, Mondher.

So if there are no more questions, I would like again to thank everyone for dialing in this morning, this afternoon. I'm very excited with again the progress we are making with our strategy. As I said, we have encouraging data with lacutamab. Our R&D is progressing nicely with new data from our ANKET platform. And we also all look forward to the continued progress, including the upcoming monalizumab presentation at ESMO this Friday. With that said, I look forward to talking to you in the new future. Thank you very much, and have a great day.

That concludes the conference for today. Thank you for participating. You may all disconnect.